Document Detail


Glutamine reduces postprandial glycemia and augments the glucagon-like peptide-1 response in type 2 diabetes patients.
MedLine Citation:
PMID:  21593352     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Impaired glucagon-like peptide (GLP-1) secretion or response may contribute to ineffective insulin release in type 2 diabetes. The conditionally essential amino acid glutamine stimulates GLP-1 secretion in vitro and in vivo. In a randomized, crossover study, we evaluated the effect of oral glutamine, with or without sitagliptin (SIT), on postprandial glycemia and GLP-1 concentration in 15 type 2 diabetes patients (glycated hemoglobin 6.5 ± 0.6%). Participants ingested a low-fat meal (5% fat) after receiving either water (control), 30 g l-glutamine (Gln-30), 15 g L-glutamine (Gln-15), 100 mg SIT, or 100 mg SIT and 15 g L-glutamine (SIT+Gln-15). Studies were conducted 1-2 wk apart. Blood was collected at baseline and postprandially for 180 min for measurement of circulating glucose, insulin, C-peptide, glucagon, and total and active GLP-1. Gln-30 and SIT+Gln-15 reduced the early (t = 0-60 min) postprandial glycemic response compared with control. All Gln treatments enhanced the postprandial insulin response from t = 60-180 min but had no effect on the C-peptide response compared with control. The postprandial glucagon concentration was increased by Gln-30 and Gln-15 compared with control, but the insulin:glucagon ratio was not affected by any treatment. In contrast to Gln-30, which tended to increase the total GLP-1 AUC, SIT tended to decrease the total GLP-1 AUC relative to control (both P = 0.03). Gln-30 and SIT increased the active GLP-1 AUC compared with control (P = 0.008 and P = 0.01, respectively). In summary, Gln-30 decreased the early postprandial glucose response, enhanced late postprandial insulinemia, and augmented postprandial active GLP-1 responses compared with control. These findings suggest that glutamine may be a novel agent for stimulating GLP-1 concentration and limiting postprandial glycemia in type 2 diabetes.
Authors:
Dorit Samocha-Bonet; Olivia Wong; Emma-Leigh Synnott; Naomi Piyaratna; Ashley Douglas; Fiona M Gribble; Jens J Holst; Donald J Chisholm; Jerry R Greenfield
Publication Detail:
Type:  Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't     Date:  2011-05-18
Journal Detail:
Title:  The Journal of nutrition     Volume:  141     ISSN:  1541-6100     ISO Abbreviation:  J. Nutr.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-21     Completed Date:  2011-08-24     Revised Date:  2012-04-20    
Medline Journal Info:
Nlm Unique ID:  0404243     Medline TA:  J Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1233-8     Citation Subset:  IM    
Affiliation:
Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Sydney 2010, Australia.
Data Bank Information
Bank Name/Acc. No.:
ClinicalTrials.gov/NCT00673894
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MeSH Terms
Descriptor/Qualifier:
Administration, Oral
Aged
Blood Glucose / metabolism
C-Peptide / blood
Cross-Over Studies
Diabetes Mellitus, Type 2 / blood*,  drug therapy*
Female
Gastric Emptying / drug effects
Glucagon / blood
Glucagon-Like Peptide 1 / blood*,  secretion
Glutamine / administration & dosage,  adverse effects,  pharmacology*
Humans
Hyperglycemia / blood,  drug therapy
Insulin / blood,  secretion
Male
Middle Aged
Postprandial Period
Pyrazines / administration & dosage
Triazoles / administration & dosage
Grant Support
ID/Acronym/Agency:
088357//Wellcome Trust
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/C-Peptide; 0/Insulin; 0/Pyrazines; 0/Triazoles; 0/sitagliptin; 56-85-9/Glutamine; 89750-14-1/Glucagon-Like Peptide 1; 9007-92-5/Glucagon

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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